Author: ["Yoh-ichi Seki","Hiromasa Inoue","Naoko Nagata","Katsuhiko Hayashi","Satoru Fukuyama","Koichiro Matsumoto","Okiru Komine","Shinjiro Hamano","Kunisuke Himeno","Kyoko Inagaki-Ohara","Nicholas Cacalano","Anne O'Garra","Tadahilo Oshida","Hirohisa Saito","James A Johnston","Akihiko Yoshimura","Masato Kubo"]
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Abstract
Members of the suppressor of cytokine signaling (SOCS) family are involved in the pathogenesis of many inflammatory diseases. SOCS-3 is predominantly expressed in T-helper type 2 (TH2) cells, but its role in TH2-related allergic diseases remains to be investigated. In this study we provide a strong correlation between SOCS-3 expression and the pathology of asthma and atopic dermatitis, as well as serum IgE levels in allergic human patients. SOCS-3 transgenic mice showed increased TH2 responses and multiple pathological features characteristic of asthma in an airway hypersensitivity model system. In contrast, dominant-negative mutant SOCS-3 transgenic mice, as well as mice with a heterozygous deletion of Socs3, had decreased TH2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of TH2-mediated allergic immune disease, and suggest that SOCS-3 may be a new therapeutic target for the development of antiallergic drugs.Cite this article
Seki, Yi., Inoue, H., Nagata, N. et al. SOCS-3 regulates onset and maintenance of TH2-mediated allergic responses. Nat Med 9, 1047–1054 (2003). https://doi.org/10.1038/nm896 